Nomura Y, Kinjo M, Tamura M
Laboratory of Supramolecular Biophysics, Research Institute for Electronic Science, Hokkaido University, Sapporo, Japan.
Neuroreport. 2000 Feb 7;11(2):301-4. doi: 10.1097/00001756-200002070-00016.
Hypoxic induction of c-fos was studied in rat brains as a function of the cerebral oxygenation state using near-infrared spectroscopy by which the hemoglobin oxygenation state and redox state of mitochondrial cytochrome oxidase could be monitored noninvasively. Following reoxygenation after hypoxia, the expression of c-fos and MAP2 mRNAs was followed by reverse transcription-coupled PCR. The expression of MAP2 remained unchanged throughout all the conditions from 21 to 8% FiO2. Under mildly hypoxia conditions, c-fos mRNA was not induced. Hemoglobin was partially deoxygenated but cytochrome oxidase remained fully oxidized. Severe hypoxia, where cytochrome oxidase was reduced, caused a significant induction of c-fos mRNA At this stage, the oxygen concentration in cerebral tissue fell to < 10(-7) M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA.
利用近红外光谱技术，在大鼠脑中研究了缺氧诱导c-fos的情况，该技术可无创监测血红蛋白氧合状态和线粒体细胞色素氧化酶的氧化还原状态，其为脑氧合状态的函数。缺氧后复氧，通过逆转录偶联PCR跟踪c-fos和MAP2 mRNA的表达。在从21%到8%的吸入氧分数的所有条件下，MAP2的表达均保持不变。在轻度缺氧条件下，未诱导c-fos mRNA。血红蛋白部分脱氧，但细胞色素氧化酶仍完全氧化。在细胞色素氧化酶还原的严重缺氧情况下，c-fos mRNA显著诱导。在此阶段，脑组织中的氧浓度降至<10(-7)M。这些数据表明氧化磷酸化的下降可能是诱导c-fos mRNA的触发因素。
